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Physiology II > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

GI tract organization

A

MUCOSA (innermost)
Epithelium
Lamina propria (contains capillaries and lacteal beds)
Muscularis mucosa

SUBMUCOSA
Meissner’s/submucous plexus enteric
nervous system (local only from small intestine to internal anal sphincter) gathers GI to force blood away from it

MUSCULARIS EXTERNA
Inner circular muscle
Auerbach’s/myenteric plexus enteric nervous system:
Outer longitudinal muscle

SEROSA

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2
Q

Piping Icing

A

Motility along the GI tract can be described as “piping icing”

The longitudinal outer layer contracts (shortens) as though you roll up your icing bag

The circular inner layer constricts the lumen as though you squeeze your icing bag

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3
Q

Unitary smooth muscle fibers of GI tract

A

GI tract contains unitary smooth muscle fibers that are connected via gap junctions to allow ion flow for
rapid, unified contractions

Once an action potential is initiated it can travel in all directions. Distance depends on excitability

No synapse but has a diffuse junction matrix coating the muscle fiber

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4
Q

ca channel signaling in smooth muscle

A

Ca channel opens
Activates calmodulin (kinase that is only active with calcium)
calmodulin phosphorylates myosin kinase
Myosin kinase in turn phosphorylates myosin

phospho-myosin binds to actin and initiates a contraction

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5
Q

Contraction and relaxation in smooth muscle

A

Is slower than in striated
Different signaling due to diffuse signaling

To relax calcium pump must be activated to pump calcium out of the smooth muscle. Must also remove the phosphate on phosphomyosin to stop the physical contraction (myosin phosphatase)

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6
Q

Gi movement

A

Slow and rhythmic.

Based on the frequency of small waves initiated by the interstitial cells of cajal

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7
Q

Slow waves

A

Not true action potentials
These are slow undulating changes in resting membrane potential

Do not cause muscle contraction but create BER
Muscle contraction occurs less than or equal to BER
Slow waves influence sodium (not calcium) to depolarize by 10mV

More slow wave potential increases the frequency of spike potentials

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8
Q

Signaling of interstitial cells of cajal

A

Set the basal electrical rhythm for each segment of the gut
3 pulses per minute in stomach
12 pulses per minute in the duodenum (may contract more as it does not have protective mucous and food must therefore move more quickly)
8 pulses per minute in the ileum

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9
Q

Slow wave peak

A

Peaks at -40mV

So when threshold occurs true action potentials occur on top of the slow wave to foster a muscle contraction

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10
Q

Spike potentials

A

True action potentials that occur on top of slow waves
Stimulated by excitable depolarization

Stretch, parasympathetic stimulation, Ach, and other GI hormones

With prolonged nervous or hormonal stimulation, increased spike potentials can lead to tonic contractions

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11
Q

Depolarization of GI muscles

A

GI spike potentials last much longer than skeletal muscle due to Ca channels that are slow to open and close

Relaxation of the smooth muscle occurs when calcium is absent and myosin phosphasae activity is present

Hyperpolarization occurs with sympathetic stimulation and norepinephrine

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12
Q

Enteric Nervous system

A

Entirely within the wall of the gut and directly synapses with cells of the GI tract
Regulate motility, secretion, absorption, and GI blood flow (all of this locally

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13
Q

Divisions of ENS

A

Auerbach’s (myenteric) plexus - directs movement

Meissner’s (submucousal) plexus directs secretion and blood flow

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14
Q

Myenteric plexus

A

Begins in the esophagus

Controls motor activity
increases tone
Increases intensity and frequency of contraction
Increases velocity of conduction (of food)

Can be inhibitory
Inhibits tonic contraction at sphincters to allow passage of food
I signals also cause an increase in the lumen diameter for of food at non-sphincter locations

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15
Q

Submucosal

A

Begins in the small intestine
Primarily controls sensory activity
Sensory receptors originating in the epithelia synapse with the meissner’s plexus to coordinate local function

secretion
absorption
submucousal motility (muscularis mucosa contracts in the submucosa to cause infoldings of the GI mucosa for secretions or blood flow

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16
Q

Signaling pathway between the branches of the NS

A

(Para)sympathetic
To myenteric plexus
to submucosal plexus (via interneuron)
to target

Hormones can increase the signaling of the myenteric or submucosal plexus

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17
Q

Visceral afferents (sensory)

A

Will relay information either locally or all the way up to the CNS
Can communicate wit prevertebral ganglion to make a prevertebral reflex. Can go up and then out to the parasympathetics.

80% of vagus fibers and 50% of sympathetic fibers are visceral afferent fibers
Some visceral afferents travel with the autonomic nerves

Percieve irritation, distention, chemicals in the gut

Must also synapse with the SNS to mediate prevertebral reflex activity in the GI tract

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18
Q

GI tract function is mostly ______ involving _______

A

Reflexive

Receptors in the mucosa (mechano and chemo) with afferent fibers to ganglia in the submucosal plexus
Interneurons that relay information between the ganglia of the 2 plexi
Efferent fibers go to the smooth muscle and glands of the GI tract

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19
Q

Ganglia of the Enteric system

A

Recieve information directly from sensory receptors in the mucosa
Sned motor fibers directly to smooth muscle or glands

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20
Q

NT of ENS

A

Dominanatly aCH

uses a large array of hormones to elicit GI responsiveness

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21
Q

ENS actions increase with PNS stimulation

A

Excitatory: increase motility and secretion

Preganglionics use aCH from brainstem
Vagus n. stimulates esophagus, stomach, pancreas, intestines through the proximal half of the colon)
And S2-4 of the pelvic nerve to stimulate distal half of intestines to the anus

Vagus can directly stimulate secretion in esophagus and stomach because there is no submucosal plexus

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22
Q

Postganglionic PNS cell bodies are in the ______ _____

A

enteric plexi
Increseases activity of the whole GI tract by stimulating the enteric plexus locally
Postganglionics release aCH or Vasoactive Intestinal Peptide or substance P

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23
Q

ENS activity decrease with SNS

A

decrease motility and secretion
From T5-L2

Preganglionics passpass through the sympathetic chain as splanchnic nerves and synapse in prevertebral ganglia

Postganglionics
Synapse with enteric NS to cause vasoconstriction and relaxation of the GI smooth muscle
CAN synapse directly with smooth muscle and glands
SNS excites the muscularis mucosa (to decrease the surface area of the epithelia)

NT is norepinephrineto generally inhibit activity and bind adrenergic receptors

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24
Q

Local reflexes

A

Initiated with
Stretch
pH
Irritants

Stimuli activate ENS afferent nerves that synpase with the enteric nervous plexi, relaying to efferent ENS to induce action of smooth muscle and glands of mucosa

Local stimuli do not activate SNS or PNS

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25
Q

Gastrocolic reflex

A

Meal causes distention of stomach that stimulates efferents, the signal goes from the SNS prevertebral ganglia to the efferent, and increases motility of the colon

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26
Q

Enterogastric reflex

A

Signals from the small intestine and colon back to stomach to inhibit stomach motility and secretions
Closes pyloric sphincter
Response from distention of duodenum

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27
Q

Colonoilieal reflex

A

Signals from colon back to ileum to inhibit emptying of ileum into colon

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28
Q

Mastication

A

chewing
Decreases the size of food
Helps mix food with saliva and mucous
Increases surface area of the food for digestive enzyme action
Surface area determines the rate of digestion

Mastication is important for the indigestible cellulose surrounding the nutrients in fruit and veggies

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29
Q

Chewing reflex

A

Presence of food in the mouth initially inhibits chewing muscles
Muscle relaxation allows depression of the mandible
Depression of the mandible initiates a stretch reflex to cause a rebound contraction against the bolus of food
Repeat

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30
Q

Saliva

A

Produced at a rate of 1.5-1 liters a day; pH 6-7
Contains
Serous secretion (ptyalin = a-amylase digests starches
Mucus secretion (mucin = lubricates/protects)

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31
Q

3 sets of salivary glands

A

Submandibular (70%) mixed serous and mucus = amylase and mucus
Parotid (25%) mostly serous = ptyalin
Sublingual (5%) serous and mucus

Lingual glands: secrete lipase to hydrolyze lipids
Buccal glands only secrete mucus

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32
Q

functions of saliva

A

Moistens and lubricates mouth for swallowing

Solvent for molecules that stimulate taste buds

Initiates digestion of carbohydrates by ptaylin (will be active through the stomach until inactivated by pH >4 from HCl)
30-40% of our dietary starches are hydrolyzed to maltose via ptyalin

Antibacterail action of lysozyme and thiocyanate ions washes away and attacks peptidoglycan layer of bacteria and thiocyanate ions disrupt ion exchange of bacteria

Secrete potassium and bicarbonate in exchange for sodium and chloride ions

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33
Q

Formation of saliva

A

Initial secretion from acinar cells is isotonic

Ductal cells modify the secretion (water impermeable)
Use Na/K ATPase to absorb sodium from the apical side. Sodium absorption causes passive chloride absorption.
Secretes potassium. Bicarbonate is actively secreted and exchanged for chloride

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34
Q

Specific breakdown of saliva formation

A

Acini cells move blood volume, water, and electrolytes with serous and mucus into the lumen of the salivary gland
The isotonic fluid then flows over the watertight ductal cells
Antiporter absorbs sodium and trades a proton (passive)
Sodium moves back to the blood through ATP hydrolysis and then trades with potassium (K is now in the secretion)
K/H exchange to lower levels of K in secretion
Cl and HCO3 antiporter removes Cl from he secretion and adds HCO3 into the lumen of the salivary gland

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35
Q

regulation of salivary secretion

A

During maximal secretion the ionic concentration changes
Increase of acini secretion twentyfold overwhelms the ion exchange and the final ionic composition more closely resembles the blood.
At lower blood rates thereis more time for ductal cells to modify the saliva, so it is optimally hypotonic to the blood

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36
Q

Salivation and P/SNS stimulation

A

PNS stimulates secretion
SNS also stimulates secretion (viscous and limited

Afferents from the tongue, mouth, and pharynx transmit a signal elicited by:
sour/acidic taste and smooth tactile sensation (increase)
rough tactile = decreased salivation

Efferents carried in CNVII and IX to the glands promotes copious secretion

signals from the CNS due to sight or smell
Reflexes stimulated by chemical irritants may stimulate saliva

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37
Q

Appetite area for the brain regulates likes and dislikes

A

Located close to parasympathetic centers in the anterior hypothalamus
Functions in response to taste and smell areas of cerebral cortex and amygdala

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38
Q

Parasympathetic pathway on salivation

A

ACh binds muscarinic receptors on acinar and ductal cells of the salivary gland
IP3 is activated and leads to a calcium flux which stimulates watery secretions (PLC -> IP3 -> Ca flux

Increases flow of blood to gland to increase saliva (more water due to increased blood flow

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39
Q

Sympathetic pathway on salivation

A

From T1-3 spinal cord levels
Nepi interacts with beta adrenergic receptors
Decreases blood flow to the glands and so there is less saliva
Less water but beta adrenergic signaling via cAMP stimulates secretion of salivary enzymes and mucus
SNS produces a viscous saliva, which is important between meals

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40
Q

Atropine

A

aCH antagonist that blocks aCH from signaling
used in conditions where heart is too slow and it must be sped up
Can block GI secretion

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41
Q

Degluttition

A

Swallowing

3 stages

Oral stage: initiates swallowing and is voluntary (by the tongue)

Pharyngeal phase is involuntary. Less than two seconds and involves a swallowing reflex to close the trachea and open the esophagus
The swallowing center then inhibits the respiratory center

Esophageal phase is involuntary and controlled by both mechanisms of the pharyngeal phase and tthe enteric nervous system. Stretch causes a reflex to cause signaling of the smooth muscle to engage in peristalsis

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42
Q

Pharyngeal stage of deglutition

A

Food moving into the opening of the pharynx stimulates an involuntary swallowing reflex
The trigeminal and glossopharyngeal sensory nerve synapses with the swallowing center spanning the medulla and pons
Motor impulses via cranial nerves 5, 9, 10, and 12 activate striated muscle involuntarily propogating swalling

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43
Q

5 steps of the swallowing reflex motor actions

A

Soft palate is pulled upward to prevent food from entering the nasopharynx
Palatopharyngeal folds approximate allowing only small pieces to enter
Vocal cords approximate and the larynx is pulled upward against the epiglottis to keep food out of the larynx and trachea
Upward movement of the larynx pulls and enlarges the opening to the esophagus and the upper esophageal sphincter relaxes
Contraction of the entire pharynx initiates peristalsis: food moves to the esophagus (the pharynx and the upper third of the esophagus are straited muscle, but this muscle is directed by involuntary reflex action

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44
Q

Esophageal stage of deglutition

A

Primary peristalsis of the esophagus is caused by involuntary peristaltic action initiated by the swallowing reflex in the pharynx and continues through the striated muscle of the esophagus and onto the smooth muscle of the lower 2/3 of the esophagus.

The cranial nerve stimulation of the pharynx is transferred to the enteric nervous system controlling smooth muscle

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45
Q

Secondary peristalsis

A

Caused by distention from food that does not pass due to primary peristalsis
percieved by visceral afferents that synapse with local myenteric response and the parasympathetic vagus nerve. This increases aCh release for continual peristaltic waves.

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46
Q

If the vagus nerve is severed

A

Enteric njervous system can still propogate secondary peristalsis in the lower 2/3 of the esophagus due to local ENS signaling

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47
Q

Delivery of food from the esophagus to the stomach requires _________

A

relaxation of the stomach.
Accomplishe dby the release of VIP (vasoactie intesitnal peptide) from the vagus and the myenteric plexus. Relaxes sphincter and smooth muscle wall to the proximal duodenum.
VIP relaxes the normally tonic constricted lower cardiac sphincter
VIP is a parasympathetic neurotransmitter that inhibits smooth muscle contraction

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48
Q

Lower cardiac sphincter and change with pressure

A

As intra-abdominal pressure increases this portion of the esophagus caves inward forming a valve

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49
Q

Paralysis of swallowing mechanism due to:

A

Damage to CN 5, 9, 10, and 12

Cranial nerve damage and swallowing center damage of the medulla are caused by infections such as poliomyelitis and encephalitis

Dystrophy of neuromuscular transmission seen in myasthenia gravis can also impair the swallowing reflex (autoantibodies bind the ACh receptor)

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50
Q

When the swallowing mechanism is partially or totally paralyzed

A

Complete interruption of the swallowing act
Failure of the glottis to close causes food to pass into the lungs instead of the esophagus
Failure of the soft palate and uvula to close posterior nares

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51
Q

Achalasia

A

Pathology of the lower esophageal sphincter
It remains contracted and refuses to relax during swallowing. This is a failure of VIP.
Food will accumulate in the esophagus and rot. Rot will lead to toxic shock and ultimately death

Caused by damage to the myenteric plexus, secondary to chronic acid reflux

Treatment with a balloon or antispasmotic drugs

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52
Q

Esophageal Secretions

A

simple mucous glands line the esophagus
Secretion is controlled by the vagus nerve

At the proximal and distal end of the esophagus compound mucus glands secrete excess bicarbonate rich mucus to protect the linign from newly swallowed food and from gastric juices

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53
Q

GastroEsophageal Reflux Disorder

A

(GERD) - Heartburn
also include chronic cough, ear/nose/throat complaints, asthma, hoarseness, anemia

Cause: Innapropriate relaxation of the lower esophageal sphincter allowing reflux of gastric content to damage the esophageal mucosa

Increased risk of Barrett’s esophageal cancer

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54
Q

GERD and anemia

A 
Chronic long term reflux
Life choices lead to a burning out of the gastro gland
Vitamin B12 (used for S phase of cell division) cannot be produced without intrinsic factor. Made from the same cell that HCl is made
55
Q

3 Main functions of the stomach

A

Storage: up to 1.5 liters - vasovagal reflex occurs when stretch receptors are activated by distention (decreases muscular tone allowing for distention)

Secretion and motility: secretions (mucus, HCL, intrinsic factor, pepsin) from gastric gland begin to digest food, peristalsis (from circular, longitudinal AND transverse layers) against the pyloric sphincter causes mixing of gastric secretion into food forming chyme

Controlled emptying of chyme: Release to the duodenum is regulated by hormones to prevent overwhelming the small intestine

56
Q

Interstitial cells of cajal in the stomach

A

Are in the body of the stomach and create a basal rhythm every 15-20 seconds
With distention of food the myenteric plexus releases ACh to stimulate action potentialscausing peristalsis

57
Q

Waves of peristalsis in the stomach

A

Multiple waves move from the stomach to the antrum but the pyloric sphincter is closed
Compound upon each other and cause a mixing action that digs deep into the walls of the lumen and propels food back to the body of the stomach

Mixing occurs for 30 minutes

58
Q

Pyloric sphincter

A

Is tonically contracted due to hormones like cholecystokinin (CCK) and secretin, and the peristaltic waves in this context increase the contraction of the sphincter

59
Q

Stomach emptying

A

The pyloris is slightly contracted and the sphincter is contracted during most of digestion
each peristaltic wave is able to psuh 2-3 mL into the duodenum so water and chyme pass with ease

60
Q

Pyloric pump

A

As the peristaltic contractions reach a threshold they overpower the pyloric sphincter and pop it open
CCK and secretin decrease and the concentration of gastrin increases and opens the pyloric sphincter

Enterogastric relex that percieves chyme will close the sphincter

61
Q

Gastrin

A

A hormone released by G-cells in response to protein and fat
Stimulate gastric motility
More motility = more opening of the pyloric sphincter

62
Q

Motilin

A

An enteric hormone that works witht eh CNS via vagal stimulation to activate a periood of intense peristalsis between meals
Used to clean the GI tract between meals and prevent food from rotting

63
Q

Motilin cycle

A

Occurs every 2 hours
is interrupted by the distention of the stomach by a meal

60 minutes of muscle inactivity
30 minutes of intensifying peristalsis
*hunger pangs may be percieved
15 minutes of rapid peristalsis
*no food present so there is no hormones closing the pyloric sphincter. No mixing action but these waves propogate through the stomach to the intestine
Transition period to quiescence
64
Q

Decrease stomach motility

A 
Enterogastric reflex (dopamine prodcution from PNS and SNS inhibit motility and gastric emptying) 
CCK is produced by I cells of the duodenum in the presence of fatty acid and/or chyme
Secretin is produced by S cells of the duodenum in the absence of acidic chyme. Inhibits gastric emptying
GIP and enteroglucagon are produced by the cells of the jejunum and duodenum in the presence of sugary and or fatty chyme. Both inhibit gastric emptying.
65
Q

Gastric secretions

A 
HCL
Mucus, salts, water, bicarbonate
Pepsinogen
Intrinsic factor
Gastrin
66
Q

Secreted HCl

A

acidifcation to optimal pH for enzymes
Secreted by parietal cells in oxyntic glands
The higher the secretory rate, the lower the pH of gastric juice.
Peak 30 mins after eating

67
Q

Secreted mucus, salts, water and bicarbonate

A

secreted by the lining of the body and antrum of the stomach to prevent corruption

68
Q

Secreted pepsinogen

A

precursor of pepsin activated by acidic pH for protein digestion. pH lower than 5
Secreted by peptic cells that are stimulated by vagus n. through distention of food

Initiates digestion and is responssibel for 20% of the process.

69
Q

Secreted intrinsic factor

A

Absorption of B12 into the colon

70
Q

Secreted gastrin

A

Regulates H secretion

71
Q

Gastric secretory structure

A

Surface mucus cells Line the the internal surface and produce a viscous and alkaline secretion nearly 1cm thick

Oxyntic or gastric glands (Deep invagination with secretory cells along the length of the structure):
mucus neck cells - mucus (top)
peptic (chief) cells - pepsinogen (bottom)
Parietal (oxyntic) cells - HCl and intrinsic factor (middle). Activated by gastrin.

Pyloric glands (In the pylorus or antrum of the stomach)
mucous cells, g cells, a few peptic cells and no parietal cells
gastrin, mucus, small amount of pepsinogen

72
Q

HCL secretion pathway

A

1) active transport of chloride by the parietal cell into the canaliculus of the gland creates the most negative potential in the body
2) sodium is attracted to the negative charge of Cl and must be actively absorbed by the parietal cell
3) Sodium is actively secreted into the ECF
4) Potassium moves into the canaliculus to neutralize the Cl
5) water splits into OH and H
6) Hydrogen:potassium antiporter exchanges H (to pair with chloride) for K
7) CO2 combines with OH to produce bicarbonate to reduce ROS actions of OH

73
Q

HCl Secretion and modern medicine

A

Proton pump inhibitors act by irreversibly blocking the hydrogen:potassium ATPase antiporter of the gastric parieal cell (aka proton pump)
The proton pump is the terminal step of HCl secretion by secreting H into the lumen

74
Q

Stimulation of gastric acid secretion

A

HCl is directly related to histamine secretion (from enterochromaffin cell)

Primary stimuli for histamine secretion:
ACh from vagus acts at muscarinic receptors to stimulate histamine from ECL cells and can stimulate parietal cells directly
Gastrin releasing peptide (food or distention) can stimulate gastrin
Gastrin from G cells in pyloric glands can also stimulate parietal cells directly or ECL cells of the gastric gland

75
Q

Inhibit HCl production

A

Decrease pH is the major control system
Low pH inhibits secretion of gastrin from G cells and this inturn inhibits HCl release. from emptying of chyme which decreases the ability to buffer H.

76
Q

Intrinsic Factor

A

Secreted by parietal cells with HCl
Required for B12 absorption in the colon

When parietal cells are destroyed
Achlorhydria - lack of stomach acid secretion
B12 deficiency - pernicious anemia (failure of RBC maturation due to lack of B12)

77
Q

Mucus production in the stomach is stimulated by

A

ACh from parasympathetic NS

Eating or food

78
Q

Phases of gastric secretion

A

Cephalic phase: 30% of HCl secretion before the meal
smell, taste, chew activates vagus to stimulate parietal cell. Vagus activates G cells to make gastrin

gastric phase: 60% of HCl secretion after a meal
Direct stimulation of parietal cells
indriectstimulation of parietal cells via gastrin
Local reflexes due to distention of the stomach
Presence of amino acids and small peptides

Intestinal phase: 10% of HCl secretion
receptors in the small intestine
Distention and presence of amino acids cause local neural reflex and gastrin production

79
Q

Gastritis

A

Common in people over the age of 50 (from mild cases to severe)
Inflammation of gastric mucosa can be caused by chronic bacterial infection (helicobacter pylori); treated with antibiotics
Ingested irritants damage protective mucosal barrier

Chronic gastritis causes gastric gland atrophy that can progressto achlorhydia and pernicious anemia due to loss of HCl and intrinsic factor

80
Q

Peptic ulcer

A

exposed area of mucosa via action of gastric/proximal small intestine
From heliobacter pyloritaht destroys mucus barrier and increases gastric acid secretion
Smoking: increased nervous stimulation
Alcohol: decrease mucus secretionand increase gastric juice
Aspirin: reduce mucus secretion due to COX1 inhibition, which creates prostaglandins to stimulate mucus production

81
Q

Pancreatic secretions

A

Digestive enzymes via acini: Digest proteins, carbohydrates, and fats
Sodium Bicarbonate via ductule/duct of acini: Neutralize acidity of chyme

Stimulated by chyme in the upper small intestine
characteristics of secretion are dependent on content of chyme

82
Q

Pancreatic zymogens

A

All pancreatic enzymes are synthesized in the pancreatic acini as zymogens
Inactive enzyme

enzymes are not activated until they reach the lumen of the duodenum (prevents pancreas from digesting itself)
Trypsin is the first enzyme activated and then goes down and activates all the other zymogens

83
Q

Pancreatic Trypsin and chymotrypsin

A

Hydrolyze proteins into polypeptides. Typically do not release AA
Recognize hydrophboic polypeptide bonds and break the chain next to that sequence

84
Q

Pancreatic Carboxypolypeptidase

A

Hydrolyses amino acids from polypeptides

The only pancreatic enxyme to release AA

85
Q

Pancreatic Elastase

A

Digests elastin fibers of muscle and other similar proteins

86
Q

PAncreatic amylase

A

digestion by amylase occurs with 15-30 minutes of chyme emptying into the duodenum
Hydrolyzes starches, glycogen, and other carbohydrates (NOT cellulose) into maltose or other small glucose polymers before chyme exits duodenum/ upper jejunum

87
Q

Fat digestion in the duodenum

A

By pancreatic enzymes:
Pancreatic lipase - hydrolyzes triglycerides into fatty acids and monoglycerides
Cholesterol esterase - hydrolyzes cholesterol esters
Phospholipase - Hydrolyzes phospholipids into fatty acids and phosphoglycerol

88
Q

Trypsin Inhibitor

A

Produced by pancreatic acini cells and prevents the activation of trypsin in the pancreas to inhibit self digestion

89
Q

Acute pancreatitis

A

With alcohol stimulatory effect or a blocked duct due to a gallstone, pancreatic tumor, or genetic mutation

60% of fat and upto 1/3 or 1/2 of proteins and carbohydrates entering the small intestine may not be absorbed
Pancreatic enzyme secretion are activated and digest pancreas within hours
Trypsin inhibitor is overwhelmed and enzymes, vasodilators and inflammatory mediators increase

90
Q

Stimuli for Pancreatic Secretion

A

Acetylcholine, GRP, and VIP
Parasympathetic vagus and cholinergic nerves int he enteric nervous system stimulate acini to favor enzymes via ACh and gastrin releasing peptide with a small amount of water and electrolytes from the ducts
Ducts are sensitive to VIP to secrete water

CCK
Secreted by duodenum and jejunum when chyme rich in protein and fats enter the small intestine
Stimulates the acini to favor enzyme secretion with a small amount of water and electrolytes from the ducts

Secretin:
Secreted by duodenum and jejunum when acidic chyme enters thew small intestine
Stimulates the ducts to favor secretion of sodium bicarbonate and water from the pancreatic duct

ALL OF THESE ARE ACTIVATED WITH THE PRESENCE OF FOOD

91
Q

CCK

A

Chyme enterign the duodenum stimulates CCK from I cells in the duodenum and upper jejunum to the blood
(products of partial protein digestion and long-chain fatty acids in chyme specifically increase CCK)

Increases secretion of pancreatic enzymes by acinar cells to foster 70-80% of total secretionof pancreatic enzymes after a meal.

Also stimulates contraction of gallbladder to secrete bile

Travels to the hypothalamus to initiate satiety. Meals too low in protein and fat will not sufficiently promote satiety

92
Q

Secretin

A

Chyme entering the duodenum stimulates the release of secretin from S cells in the duodenum and upper jejunum into the blood
Chyme with a pH of >3-4 specifically stimulates secretin

Provides appropriate pH for pancreatic enzymes (7-8)
Secretion of large amounts of bicarbonate from pancreatic ductules to neutralize acidic stomach chyme
Stimulates watery bicarbonate secretion from the bile ducts

Prevents duodenal ulcers

93
Q

Pancreatic secretion of bicarbonate ions and water ions

A

Epithelial cells of the bile ducts and pancreas have a secretin receptor
Activates carbonic anhydrase to create bicarbonate
Bicarbonate will then move out to the lumen through bicar-chloride antiporter
Creates a bicarbonate ion concentration 5 times higher than in plasma and water will follow.
Creates a strong electircal imbalance so taht Na follows as well (Na and water move through the tight junctions

94
Q

Cystic fibrosis patients

A

Can’t shuttle chloride into the lumen. This inactivates bicarbonate:chloride antiporter. Watery secretions are lower in the CF patients and they need to take supplemental pancreatic enzymes and bile

95
Q

Phases of pancreatic secretion

A

Same as in the stomach
Cephalic and Gastric Phases
Same nervous signals that cause secretion in the stomach also cause vagal ACh release in the panceras
Only small amounts of pancreatic secretion reaches the duodenum due to lack of significant fluid secretion

Intestinal phase
After chyme enters the small intestine, pancreatic secretion becomes copious, mainly due to secretin

96
Q

Bile

A

Secreted continuously up to a 600 ml - a liter a day

Mostly amphipathic (region of charge and a region of neutrality) bile salts, 1/2 of total solutes
Cholesterol, bilirubin, lecithin, hormone metabolites, metabolites, and electrolytes of plasma
97
Q

Functions of bile

A

Fat digestion and absorption
Amphipathic molecule emulsifies large fat molecules into smaller particles to increase the surface area for water soluble enzymes to digest fat
Also a chaperone for digested fat end products to the intestinal mucousal membrane (w/o bile salts 40% of ingested fats would be lost in feces)

Excretion of waste from blood
Bilirubin (end product of hemoglobin destuction) and excess cholesterol

98
Q

Bile synthesis and secretion

A

Dominantly composed of a chemically modified cholesterol called taurocholic acid. an amphipathic molecule
Bile is continuously secreted from hepatocytes into canaliculi, larger bile ducts of the liver, and into the hepatic and common bile duct. Bile can flow directly into the duodenum or can be directed into the gallbladder by the cystic duct.

99
Q

Secretin and bile

A

Under secretin the bile fluid can increase by 100%

100
Q

Gallbladder and bile

A

75% of bile produced is stored in gall bladder. Loss of gallbladder make it difficult to digest high fat foods.
450ml of bile is produced by hepatocytes in 12 hours.
Gallbladder can concentrate this down to 30-60ml.
the epithelia of the gallbladder absorbs water, sodium, chloride, and other electrolytes to concentrate the bile

101
Q

Emptying the gallbladder

A

When chyme enters the duodenum, CCK is released to the blood and stimulates rhythmic contractions of gallbladder

ACh from the vagus and enteric system can also empty the gallbladder

102
Q

Recycle of bile salts

A

90% of bile salts are reabsorbed from the small intestine into the portal blood and liver to be resecreted into bile
Bile salts repeat the circuit about 17 times before being carried out into the feces

103
Q

Cholesterol gallstones

A

during bile salt secretion, about 1-2 grams of cholesterol are removed from blood and secretedinto bile each day

Causes
Too much absorption of water from bile
too much absorption of bile acids from bile
Too much cholesterol in bile
Inflammation of epithelium
104
Q

BER of small intestine is

A

12 contractions per minute but decreases caudad
High BER creates a series of peristaltic contractions that cause a segmentation or chopping of the Small Intestines in which one wave relaxes and another begins

Visceral afferents detect the location of food and alternately release different NT’s to accomplish the above effect

105
Q

ACh, Serotonin, and substance P in Small Intestine

A

cause contraction orad to the distention

Blocks upstream movement

106
Q

VIP and Nitric Oxide release in Small Intestine

A

Cause relaxation caudad to the distention

107
Q

Movements of the Small Intestine

A

Controlled by distention beginning with the entry of chyme and the gastroenteric reflex initiated by the distention of the stomach

108
Q

Gastroileal Reflex

A

Intensifies peristalsis and forces chyme into the cecum past the ileocecal valve

109
Q

SI movement is increased by

A

Gastrin, CCK, insulin, motilin, and serotonin

110
Q

SI movement decreased by

A

Secretin and glucagon

111
Q

Peristaltic rush

A

Intense irritation of SI mucosa, often caused by infections, chemicals, or excessive distention

Quickly dilutes the pollutant and moves it through the tube

initiated by stimulation of the myenteric plexus and mediated by reflexes in the autonomic NS and brainstem

112
Q

Brunner’s Glands in the duodenum make mucus in response to

A

Tactile/irritating stimuli on duodenal mucosathat activates the meissner’s plexus (also S, I, L, M, K cells)
Vagal stimulation (augment secretion of meissner’s plexus)
Secretin
Inhibited by sympathetic stimulation (50% of ulcer patients have sympathetic dominance)

113
Q

Function of SI mucus

A

Protects duodenum from digestion by acidic chyme

Excess bicarbonate, adding to bicarbonate from pancreatic secretion and bile to neutralize HCl

114
Q

Crypts of the small intestine

A

Crypts of Lieberkuhn and villi of the Si are covered by two types of secretory cells
Goblet cells: secrete mucus to lubricate and protect
Enterocytes: crypts secrete water and electrolytes and villi reabsorb water and electrolytes, and metabolites

115
Q

Chemotherapy on epithelial cells of SI crypts

A

If the chemotherapy affects mitosis there can be deficits to these cells as they regularlly undergo mitosis and have a life span of 5 days.
May be associated with mucousal damage

116
Q

Fluids secretion/absorption at SI

A

Absorbs about 7 liters a day (passes 2l to the LI)

2L per day of intestinal secretions are formed in the crypts. Isotonic to ECF and slightly alkaline. Aids in absorption of nutrients into the blood.
Secretes sodium to facilitate the absorption of carbohydrates and protein back intot he blood

117
Q

Si secretion stimulated by

A

Prostaglandins, ACh, VIP, and serotonin

118
Q

SI secretion paths for molecules

A

Chloride and bicarbonate secretion to thje lumen supportsosmotic movement of water between tight junctions of the epithelia

119
Q

Constipation in cystic fibrosis

A

There is a defect in the Chloride transport protein on the apical side

120
Q

SI absorption

A

Only monomers of fat, protein, carbohydrate, nucleotide are absorbed to the blood

121
Q

Digestive enzymes in the SI

A

Peptidases split peptides into amino acids (can also be active in the cytoplasm of epithelia cells)
Sucrase, maltase, isomaltase, and lactase split disaccarhides into monosaccharides
Lipase splits neutral fat into glycerol and fatty acids

122
Q

digestion occurs via

A

hydrolysis
very specific process for each enzyme (starch has a-1,4; cellulose has b-1,4 bonds)
except for cellulose. humans do not possess cellulase so this function is taken up by some gut flora (LI, ileum)to allow some digestion of cellulose

123
Q

Three major sources of carbs in human diet

A 
Sucrose = dissaccharide in cane sugar
Lactose = dissaccharide in milk
Starches = large polysaccharides in non-animal food
124
Q

Hydrolysis of carbohydrates

A

Lactose to galactose and glucose
sucrose to fructose and glucose
maltose and others into glucose

80% glucose and 10% galactose and fructose each

125
Q

Hydrolysis of proteins

A

pepsin of teh stomach and trypsin, chymotrypsin and procarboxypolypeptidase hydrolyze proteins to polypeptides
Most protein remains as tri- or di-peptides after pancreatic activity

hydrolysis by eptidases occurs along the brush border of the SI and in teh cytoplasm of enterocytes lining the villi. The last digestive stage of protein

Most final products are aa
Leaky gut, allergy and other immune responses may occur if protein is absorbed in excess

126
Q

Hydrolysis of lipids

A

most abundant animal fats are triglycerides.
Less than 10% of triglycerides are hydrolyzed by lipase secreted by lingual glands and swallowed with saliva (90% of fat digestion occurs in the small intestine)
Hydrolysis occurs on the surface of lipids (water insoluble).
Bile breaks down lipids
Most important enzyme is pancreatic lipase
bile salts form micelles to transport monoglycerides and FFA to the brush border of SI for absorption of both

127
Q

Total Fluid absorbed each day by the small intestine

A 
Ingested fluid 1.5L
Salivary secretions 1.5L
Gastric Secretions 2.5L
Pancreatic and bile secretion 2L
Small intestine secretions 1L
128
Q

Folds of kerckring

A

Increase the surface area of teh SI 3X
Millions of small villi that increase another 10X
Brush border on the villi increase SA another 20X

129
Q

Absorption of water and ions in the SI

A

Water is absorbed by osmosis
To accomplish this the SI and Li absrob 25-35g of sodium a day (extreme diarrhea will deplete stores of sodium to lethal levels in hours) less than .5% is lost to feces usually

130
Q

Aldosterone and sodium absorption

A

Greatly enhances sodium absorption especially in the colon and it does not allow water loss in feces.
In dehdration aldosterone causes constipation

131
Q

Absorption of nutrients from the SI each day

A 
Several hundred grams from SI each day 
100 g fat
50-100g amino acids
50-100g ions
7-8 liters of water
132
Q

Absorption of carbs in the SI

A

80% of carbs absorbed are glucose monomers
Transported via a sodium co transport system (w/o sodium no glucose is absorbed). SGLT1 requires sodium binding first before glucose can bind for transport (SGLT2 in kidney) in the jejunum specifically.

GLUT2 moves the glucose from inside the cellto the blood> Use sodium potassium ATPase to move Na into the blood

galactose can also bind SGLT1

Fructose binds GLUT 5 and moves via facilitated diffusion w/o sodium

133
Q

Absorption of proteins in the SI

A

After crossing teh apical membrane (via peptide transport protein) the (???)peptides are broken down by cytoplasmic enzymes and the basal side of teh epithelia release 99% aa

AA use a sodium cotransporter. thos ethat do not use this move via facilitated diffusiondepends on the R-group of the amino acid

134
Q

Absorption of fat in SI

A

Lipid hydrolysis occurs to create monoglycerides and FFA. Forms micelle with bile salt
Without bile micelles only 40-50% of fat is actually absorbed
Bile will go to portal vein for recycling. FFA and monoglycerides are taken u0p by the ER to make tryglycerides. Then the lipids are formed into a chylomicron with cholesterol and then move to the lacteal and then enter the blood at the thoracic duct

Malabsorption tropical sprue

Physiology II (4 decks)

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